The role of IL-12p40 during host cell infection with Yersinia pestis KIM D27 (45.22)

Abstract Yersinia pestis, a facultative intracellular pathogen, is the causative agent of plague. A previously developed vaccine model using Yersinia pestis KIM D27, B cell-deficient mice, and convalescent serum resulted in the generation of T cell-meditated protection against lethal pneumonic infec...

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Published inThe Journal of immunology (1950) Vol. 182; no. 1_Supplement; pp. 45 - 45.22
Main Authors Parent, Michelle A., Joerger, Torsten A., Golwala, Sohil N., Smiley, Stephen T., Blumerman, Seth L.
Format Journal Article
LanguageEnglish
Published 01.04.2009
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Summary:Abstract Yersinia pestis, a facultative intracellular pathogen, is the causative agent of plague. A previously developed vaccine model using Yersinia pestis KIM D27, B cell-deficient mice, and convalescent serum resulted in the generation of T cell-meditated protection against lethal pneumonic infection. In order to understand how this serum results in the development of protective T cells we investigated the interaction between the host immune response, convalescent serum and Y. pestis. First, we determined that IL-12p40 but not IL-12p35 was required for mice to survive this vaccination regimen. We then began to examine the early host response to infection by studying dendritic cells (DC) infected with Y. pestis in the presence of convalescent serum, since DC are cable of presenting antigen to naïve T cells. We infected cultures of bone marrow-derived DC and established that Y. pestis is able to infect DC. Interestingly, convalescent serum does not result in clearance of organisms but sustains infection. Currently, we are investigating cytokine production and cell surface maker expression profiles in Y. pestis infected DC. Preliminary data of infected DC in the presence of convalescent serum results in an increase in IL-12p40 gene expression. Our goal is to ascertain those events occurring early during the course of host infection that lead to generation of this cell-mediated protection. This research is supported by a grant from the University of Delaware Research Foundation.
ISSN:0022-1767
1550-6606
DOI:10.4049/jimmunol.182.Supp.45.22